modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway.

The aim of this study was to investigate and expression and their effect on autophagy in hepatocellular carcinoma (HCC). We found that expression was low in hepatoma tissues and cells. Overexpression of decreased the activity of hepatoma cells. To analyze autophagic flux, we monitored the formation of autophagic vesicles by fluorescence protein method. Autophagy-related protein LC3B-II was accumulated and P62 was decreased, which indicated that autophagy was induced by BECN1, while could suppress this trend. Immunofluorescence assay showed that and Beclin 1 were co-located in hepatoma cells. Immunoprecipitation showed that could inhibit the autophagy of hepatoma cells by combining with Beclin 1. ELISA and co-immunoprecipitation suggested that the combination between BCL2L10 and Beclin 1 reduced the bond between Beclin 1 and PI3KC3. Based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PI3K/AKT signaling pathway was significantly upregulated in HCC. In conclusions, had a low expression in HCC tissues and cells, which could release to induce autophagy of hepatoma cells by downregulating PI3K/AKT signaling pathway.